Search PubMed⌕ Search

Biomedical subjects

G Vassort

Publications and source records attributed to G Vassort.

At least 109 records · Page 6Linked to original sources
PubMed1979

Sodium-calcium exchange in regulation of cardiac contractility. Evidence for an electrogenic, voltage-dependent mechanism.

The origin and regulatory mechanisms of tonic tension (Ca current-independent component of contractility) were investigated in frog atrial muscle under voltage-clamp conditions. Tonic tension was elicited by depolarizing pulses of 160 mV (Em = +90 mV, i.e., close to E ca) and 400--600 ms long. An application of Na-free (LiCl) or Ca-free Ringer's solutions resulted in a fast (less than 120 s), almost complete abolition of tonic tension. When [Na]o was reduced (with LiCl or sucrose as the substitutes), the peak tonic tension increased transiently and then decreased below the control level. The transient changes in tonic tension were prevented by using low-Na, low-Ca solutions where the ratios [Ca]0/[Na]40 to [Ca]o/[Na]4o were kept constant (1.1 X 10(-8) mM-3 to 8.7 X 10(-13) mM-5). Na-free (LiCl) solution elicited contractures accompanied by a membrane hyperpolarization or by an outward current even when the Na-K pump was inhibited. 15 mM MnCl2 (or 3 mM LaCl3) inhibited the development of the Na-free contracture and the related part of hyperpolarization or the outward current. In conclusion, our results indicate that tonic tension is regulated by a Na-Ca exchange mechanism. Furthermore, they suggest that this exchange could be electrogenic (exchanging three or more Na ions for one Ca ion) and thus voltage dependent. The possible contribution of an electrogenic Na-Ca exchange in the maintenance of cardiac membrane potential is discussed.

Animals↗
PubMed1979

Transmembrane calcium movements and excitation-contraction coupling in myocardial cells.

It has been realized for a century that Ca2+ is important in the initiation and the control of mechanical activity. The present paper does not cover the field of excitation-contraction coupling in heart but mainly reports some modern and controversial aspects about the regulation of the internal Ca concentration by the sarcolemma while the role of internal stores is only discussed. The first part deals with flux experiments; the second with the slow inward current mainly carried by Ca ions. An analysis of the mechanical activity reveals that only a part of tension is triggered by this slow current; besides, a second component of tension is demonstrated and an exchange mechanism of Na and Ca ions is described in detail. This countertransport, during depolarization, facilitates an influx of Ca ions (coupled to an efflux of Na ions). During hyperpolarization, or even at the resting membrane potential, it promotes an efflux of Ca ions. Thus, the same mechanism may account in part for the development or for the relaxation of tension according to the membrane potential.

Action Potentials↗
PubMed1979

Is there a voltage-dependent Cl conductance or do Cl ions modify other conductances in crab muscle fibre?

1. The electrical activity of crab muscle fibre disappeared in Cl-deficient solutions when Cl was substituted by an impermeant anion. 2. Under voltage-clamp conditions, the above solutions abolished Ca-inward current and altered K-outward currents. 3. In 84 mEq-Cl solutions, (Cl substituted by methane sulfonate or proprionate) it is chiefly in gCa-availability that was modified. Half-availability was shifted by 50 to 70 mV in a hyperpolarizing direction while the slope factor was noticeably increased. Similar effects, but of less amplitude, were observed when decreasing the external Cl concentration to 255 mEq. 4. Ca- and slow K-activation variables were shifted by 17 mV and 20 mV respectively in a hyperpolarizing direction by the Cl-poor (84 mEq) solution. Cl-deficiency was even more efficient on the fast outward current than on the Ca current; the former current could be significantly reprimed only if the Cl-concentration was reduced by about 10 per cent. 5. In Cl-deficient solution, electrical activity could be restored by injecting hyperpolarizing currents in order to reprime the Ca-conductance. 6. It is suggested that Cl-ions bind to positive charges on both sides of the membrane. When substituted by impermeant anions, the local anion concentration decreases at the internal surface of the membrane, thus reducing the strength of the effective field of the membrane.

Animals↗
PubMed1976

Calcium conductance in relation to contractility in frog myocardium.

1. Ca inward current and the corresponding phasic component of tension were measured in frog atrial muscle under voltage-clamp conditions in Na-free (Li) Ringer solution with tetrodotoxin (TTX) added. 2. The quantity of Ca ions entering the cell upon depolarization, delta[Ca]i, was linearly related to peak phasic tension. 3. The voltage dependence of the steady-state inactivation of the Ca-carrying system, f infinity, against voltage yielded similar relationships whether determined directly from variations of Ca inward current or peak phasic tension. The Ca system was almost fully available at potentials more negative than -45 mV and almost fully inactivated at potentials more positive than +10 mV. 4. It was established that the time- and voltage-dependence of Ca current and of phasic tension are directly related. The time constants of Ca activation, tau f, were comparable in the range of membrane potential investigated (-20 to +25 mV), whether determined directly from the decay of Ca current or indirectly from peak phasic tension. 5. It was concluded that the Ca current, ICa, directly activates phasic contraction and that either parameter can be used as an indicator of the kinetics of the Ca-carrying system. Peak phasic tension was used to determine tau f further in the membrane potential range in which interference by other membrane currents renders direct analysis of Ca current difficult. 6. The tau f against voltage relationship determined from phasic tension showed that the inactivation process of the Ca-carrying system is slowest at membrane potentials around -13 mV (tau f = 55 msec) and that the rate of inactivation increases with both increasing and decreasing depolarizations. 7. It is suggested that normal repolarization in frog myocardium depends mainly on the decay of Ca inward current rather than on an increase of outward current.

Action Potentials↗
PubMed1975

Initial and delayed membrane currents in crab muscle fibre under voltage-clamp conditions.

Membrane currents are investigated under voltage-clamp conditions in crab muscle fibre. 2. Step depolarizations elicit an initial composite current followed by a late outward current. 3. One of the components of the initial current is inward. It is sensitive to the external calcium concentration and inhibited by manganese ions, it can be carried also by strontium ions; thus it is expected to be a calcium current. 4. In TEA solution this calcium current appears alone, it reverses when the membrane polarization is carried beyond an internal potential of +30 or +35 mV. Such a low equilibrium potential for calcium ions can be explained either by a low selectivity of the calcium channel or by a local accumulation of calcium ions. 5. Calcium conductance shows voltage- and time dependence. 6. The late outward current corresponds to a potassium current and is inhibited by TEA ions. Its activation exhibits voltage- and time dependence. 7. The activation curve of the late potassium current is shifted in a depolarizing direction by addition of manganese ions. A similar shift produced by increasing [Ca]o or decreasing [Ca]i has been described on other preparations. It is then supposed that the electrical field of the membrane is modified by the gradient of double cations.

Animals↗
PubMed1975

Evidence for a transient potassium membrane current dependent on calcium influx in crab muscle fibre.

1. Voltage-clamp experiments were achieved on crab muscle fibre with the double sucrose-gap technique. 2. The accuracy of the imposed voltage has been controlled with an impaled micro-electrode connected to an external circuit. 3. Step depolarizations elicit two kinds of records. In type I fibres, the initial current exhibits only an inward calcium component. In type II fibres, the initial current exhibits a hump, transient outward current, mixed with the calcium current; these fibres exhibit always action potentials with fast repolarization. 4. A potassium origin is suggested for this outward current, due to its dependence on [K]o and its inhibition by TEA. 5. In fibres with a composite initial current, the voltage dependence of the availability of the measured inward current appears complex. It can be shown to be the sum of a simple calcium inactivation (which is observed alone in TEA solution) and a fast potassium inactivation. This potassium conductance is nearly half-available at the resting membrane potential. 6. The origin of the transient outward current is tentatively described. Consecutive to a transient internal increase of calcium ions (due to the calcium current) its activation curve is shifted in an hyperpolarizing direction resulting in an increased activation for an apparent identical depolarization. 7. This fast outward current which overlaps the calcium inward current can account for the low amplitude and the variability of the electrical activity of crab muscle fibres.

Action Potentials↗
PubMed1975

Voltage-clamp analysis of transmembrane ionic currents in guinea-pig myometrium: evidence for an initial potassium activation triggered by calcium influx.

Voltage-clamp analysis of ionic transmembrane currents in very small strands of guinea-pig myometrium was carried out with a double sucrose-gap technique. It was found that the electrical activity, consisting of a spike followed by a long plateau, is controlled by, at least, four ionic conductances. (1) A fast inward current is responsible for the spike generation. Its low equilibrium potential accounts, partly, for the low amplitude of the spike. (2) The fast inward current is antagonized by an early outward current which occurs almost simultaneously. This fast outward current is blocked by TEA. Its reversal potential is about -95 mV. A tenfold increase in the external K-concentration shifts the reversal potential by 50 mV. Thus, it is concluded that the initial outward current is carried by K+. (3) A slow current, whose reversal potential ranges from -40 to -10 mV, is responsible for the negative after-potential. Cl-depletion (to one-ninth) does not modify this current while Na-depletion (to one-ninth) decreases its reversal potential by about 20 mV. (4) A late current which shows delayed rectification is elicited by long pulses. Its analysis is made difficult by the change mainly of the K-equilibrium potential suggesting accumulation of K+ outside the cell membrane. (5) The availability of the inward current and of the slow current, determined in TEA solution, shows that both currents are half-inactivated by a 8 mV conditioning depolarization. Using a slope factor of -2-5 or -3 the availability curve fits the experimental values. In normal solution, the availability curve of the initial current appears complex in the hyperpolarization range. The fast outward current, which is partly inactivated at the resting potential, is restored by conditioning hyperpolarization and then antagonizes the Ca inward current more. (6) It is concluded that the fast K-current controls the spike generation and accounts for the fast repolarization of the spike. The fast and transient increase in K-conductance may be the result of a momentary local increase in Ca concentration at the internal surface of the membrane.

Action Potentials↗
PubMed1975

Transmembrane sodium movement and regulation of contraction in frog atrial muscle during the inotropic effect of veratrine.

In this study, voltage clamp experiments to determine membrane conductance changes revealed that veratrine slowed considerably inactivation of the Na system, thereby greatly increasing Na inward current. The contractile response (registered simultaneously with membrane currents) was closely related to this increase: applying tetrodotoxin (TXX) or Na-free (sucrose) Ringer's solution abolished the effect of veratrine on electrical and mechanical activity almost simultaneously. With Na-free (LiCl) Ringer's solution the effect of veratrine on membrane current was obtained, but the mechanical response was unchanged. Thus transmembrane movement of Na ions is involved in regulation of contraction during the inotropic effect of veratrine. As veratrine did not substantially change the slow Ca inward current, inotropic action seems dependent on some intracellular stores of Ca ions. The possibility that intracellular Na ions govern the amount of intracellular Ca ions available for the development of the inotropic effect of veratrine is discussed.

Action Potentials↗